With the ageing of populations, the management of
osteoporosis is a priority of society in general.
Epimedin B, a major ingredient of Herba
Epimedii, which has the advantages of high content and hypotoxicity has been proved to be effective in preventing
osteoporosis in vitro. However, the efficacy and mechanism of
Epimedin B on
osteoporosis in vivo have not been well elucidated yet. This study aimed to investigate the effects and the potential mechanisms of 8-week repeated
oral administration of
Epimedin B (10 and 20 mg/kg/day) on a mouse
osteoporosis model. Effects of
Epimedin B were evaluated by examinations of serum bone turnover markers, bone mineral density, bone microstructure parameters and histopathological section.
Epimedin B significantly rose N-terminal propeptide of
type I procollagen (P1NP) and dropped
C-telopeptide of
type I collagen (CTX1). Connectivity density (Conn.D) increased significantly while structure model index (DA) decreased significantly after treated by
Epimedin B. Meanwhile,
Epimedin B administration significantly increased the number of trabecular bones while significantly decreased the gap between them. Overall,
Epimedin B showed beneficial effects on
osteoporosis. Furthermore,
RNA sequencing-based analysis revealed 5 significantly down-regulated transcripts and 107 significantly up-regulated transcripts between the
Epimedin B administration group and the model group. These transcripts were mapped to 15 pathways by KEGG enrichment analysis, of which PI3K-Akt signalling pathway, MAPK signalling pathway and
PPAR signalling pathway were most connected to
osteoporosis. To conclude,
Epimedin B is effective in treating
osteoporosis in mice via regulating PI3K-Akt, MAPK and
PPAR signalling pathway.